Mechanical properties of myocardium from hypertrophied rat hearts. A comparison between hypertrophy induced by senescence and by aortic banding.
- 1 February 1980
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 46 (2) , 292-300
- https://doi.org/10.1161/01.res.46.2.292
Abstract
Cardiac hypertrophy is a characteristic change that occurs in senescence. Muscles from senescent compared to mature hearts demonstrate functional alterations that are similar to the alterations found in muscles from experimentally hypertrophied hearts. Functional alterations in senescent muscles may be related to the underlying hypertrophy. A rat model of aging in which experimental hypertrophy was produced by aortic banding was used. The time course and extent of cardiac hypertrophy, isometric twitch and viscoelasticity parameters as a function of age were determined in muscles from the rat hearts. Aortic banding was performed on middle-aged rats to produce the same extent of hypertrophy as seen in the senescent hearts. The resulting functional alterations in muscles from the banded (B) hearts were compared to the senescent (S) and middle-aged (M) muscles. Using tibial length as a reference 14% LV [left ventricle] hypertrophy was found in senescent compared to both young and middle-aged rats, indicating that the hypertrophy occurred during the last quarter of life. The S muscles demonstrated a 25% prolongation in contraction duration (CD) and a 30% increase in slope of the active stiffness-tension line (.alpha.A) compared to young adult and middle-aged muscles. Compared to middle-aged muscles the B muscles demonstrated a similar spectrum of change in mechanical properties as the S muscles (8% increase in CD and 15% increase in .alpha.A) but the quantitative differences between the B and S muscles were significant. Over the functional range of developed tensions the B muscles demonstrated the lowest and the S muscles the highest values of stiffness. A portion of the mechanical property alterations seen in the senescent heart apparently are due to the underlying hypertrophy. Hypertrophy produced by mechanical loading of the LV cannot explain all of the senescent changes.This publication has 24 references indexed in Scilit:
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